8 research outputs found

    Initiation of mucosal innate immune response via dendritic cells against <i>Toxoplasma gondii</i> infection in mice.

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    <p>The toll-like receptor (TLR)-adaptor protein MyD88 is a key element to the protective response based on production of IL-12. Secretion of IL-12 will trigger an effective cellular-based immune response with production of INF-γ and activation of a Th1 T lymphocyte profile. (A) This innate response is mainly dependent on TLR11, which forms endolysosomal dimers with TLR12 that recognize profilin from <i>T</i>. <i>gondii</i>. This recognition is central to mucosal immunity triggering production of IL-12. (B) In the absence of TLR11, however, this response is still minimally and sufficiently compensated by indirect stimulation provided by the gut microbial commensals via TLR2, TLR4, and TLR9 [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0004176#pntd.0004176.ref044" target="_blank">44</a>]. In this case, infection-induced cell destruction and intestinal dysbiosis apparently trigger loss of tolerance to gut commensals. When the gut microbiota is severely reduced by prolonged antibiotic treatment, the following observations can be made: (C) Wild-type mice expressing TLR11 exhibit a reduced but not abolished IL-12 response. These animals can still build up Th1 immunity. (D) TLR11-knockout mice are unable to mount IL-12 responses against this parasite, and Th1 immunity is severely impaired. In conclusion, gut commensals serve as natural molecular adjuvants during <i>T</i>. <i>gondii</i> infection.</p

    Additional file 3: of Spliceosomal introns in Trichomonas vaginalis revisited

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    Figure S1. Experimental validation of the 62 T. vaginalis putative introns by RT-PCR. These introns were categorised as (a) functional, (b) non-functional or (c) undetermined. (PDF 256 kb

    The microbiota of the human gut and vagina and the site-specific associated parasitic protozoans.

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    <p>The bar chart illustrates bacterial diversity at species level, grouped by phylum, found in the gut (top bar) [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0004176#pntd.0004176.ref004" target="_blank">4</a>] and vagina (bottom bar) [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0004176#pntd.0004176.ref009" target="_blank">9</a>]. Bacterial phyla found in the gut are, from left to right: Actinobacteria, Bacteroidetes, Firmicutes, Proteobacteria, and the least diverse group of Fusobacteria. Bacterial phyla found in the vagina are, from left to right: Actinobacteria, Bacteroidetes, Firmicutes, and Fusobacteria. Despite showing higher species diversity in comparison to the vagina, the relative abundance of bacterial species in the gut varies greatly among individuals [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0004176#pntd.0004176.ref005" target="_blank">5</a>]. In the vagina, however, the microbiome can be categorized into five microbial communities as illustrated in the pie chart. Four of these are dominated by a single species of <i>Lactobacillus</i> (phylum Firmicutes). These species, coloured in blue, are shown on the pie chart from top to bottom in an anticlockwise direction: <i>L</i>. <i>jensenii</i>, <i>L</i>. <i>crispatus</i>, <i>L</i>. <i>gasseri</i>, and <i>L</i>. <i>iners</i>. A fifth community, coloured in yellow, is composed of a highly diverse polymicrobial community containing mostly anaerobic bacteria such as <i>Prevotella bivia</i>, <i>Atopobium vaginae</i>, <i>Gardnerella vaginalis</i>, <i>Megasphaera</i> sp., and <i>Sneathia</i> sp., [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0004176#pntd.0004176.ref009" target="_blank">9</a>]. Parasitic protozoans of human gut and vagina are listed on the left. The only vaginal protozoan of humans is the extracellular parasite <i>Trichomonas vaginalis</i>. Except for the extracellular parasite <i>Entamoeba histolytica</i> and the intracellular parasite <i>Toxoplasma gondii</i>, these protozoans are site-restricted and cause self-limiting infections. The interplay of these parasites with the human microbiota is discussed in this review.</p

    Additional file 1: of Spliceosomal introns in Trichomonas vaginalis revisited

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    Table S1. Primers used in this study to validate the putative introns by RT-PCR. Nucleotides that target 5' and 3' UTRs were indicated with lower-case letters. Underlined bases are located outside the transcribed region of these genes. (PDF 36 kb

    Additional file 6: of Spliceosomal introns in Trichomonas vaginalis revisited

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    Figure S2. Evidence of gene transcription and mRNA splicing for the 13 putative introns that could not be experimentally determined in this study. (PDF 1422 kb

    Additional file 2: of Spliceosomal introns in Trichomonas vaginalis revisited

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    Table S2. An update on the gene ID of the 42 introns previously reported, with references as indicated [15, 16]. (PDF 77 kb

    Additional file 5: of Spliceosomal introns in Trichomonas vaginalis revisited

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    Table S4. T. vaginalis genome segments that match the consensus sequence of type B intron (GTWYWDN{7}TCTAACH{1,2}AACAG). (PDF 85 kb

    Additional file 4: of Spliceosomal introns in Trichomonas vaginalis revisited

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    Table S3. T. vaginalis genome segments that match the consensus sequence of type A intron (GYAYGYN{41,178}RCTAACACAYAG). (PDF 84 kb
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